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Human bladder cancer cell line high throughput sequencing - genes regulated by hMSH2 - CDDP therapy

ABSTRACT: The activation status of some DNA damage repair proteins is closely related to the efficacy of CDDP chemotherapy in MIBC. In this study, we used CRISPR/cas9 gene-editing technology to construct hMSH2-deficient bladder cancer cells and confirmed that loss of hMSH2 decreased the sensitivity of bladder cancer cells to cisplatin. Transcriptome analysis was performed to find the potential genes that could be regulated by hMSH2.

ORGANISM(S): Homo sapiens

PROVIDER: GSE193753 | GEO | 2024/06/20

REPOSITORIES: GEO

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Human bladder cancer cell line high throughput sequencing - genes regulated by hMSH2 - untreated

Project description:The activation status of some DNA damage repair proteins is closely related to the efficacy of CDDP chemotherapy in MIBC. In this study, we used CRISPR/cas9 gene-editing technology to construct hMSH2-deficient bladder cancer cells and confirmed that loss of hMSH2 decreased the sensitivity of bladder cancer cells to cisplatin. Transcriptome analysis was performed to find the potential genes that could be regulated by hMSH2.

2024-06-20 | GSE193754 | GEO

APIM-peptide targeting PCNA improves cisplatin therapy in a rat muscle-invasive bladder cancer model

Project description:High mortality rate of muscle-invasive bladder cancer (MIBC) and complexity of disease demand new multi-targeting treatment strategies. Targeting proliferating cell nuclear antigen (PCNA) with a peptide containing the AlkB homologue 2 PCNA interacting motif (APIM), is shown to impair multiple vital cellular stress responses and induce hypersensitivity against several chemotherapeutics in different pre-clinical models. This study examine the anti-cancer efficacy of the novel APIM-peptide drug when combined with cisplatin-based therapies (cisplatin, cisplatin/gemcitabine (GC) and methotrexate/vinblastine/adriamycin/cisplatin (MVAC)) in a panel of bladder cancer (BC) cells and with intravenous cisplatin-therapy in a rat MIBC-model. Furthermore, we explore the molecular mechanisms underlying the observed effects on a genomic, proteomic and metabolomic level using microarray, multiplexed inhibitor bead (MIB)-assay, and targeted mass spectrometric metabolite profiling. The APIM-peptide significantly increased the efficacy of all cisplatin-based therapies in all BC cell lines tested, including a cisplatin resistant cell line and reduced the tumor load in cisplatin treated MIBC-bearing rats. Genome and proteome analysis of APIM-peptide/cisplatin treated BC cells revealed reduced expression of multiple proteins frequently overexpressed in MIBC. Of notice, the EGFR/ERBB2, PI3K/Akt and MAPK signaling pathways and anti-apoptosis were downregulated. We suggest that the anti-cancer effect of the APIM-peptide is through the downregulation of several known oncogenic signaling pathways including anti-apoptosis. Together our results indicate that the APIM-peptide represents a potential improved treatment approach for patients with MIBC.

2018-09-10 | PXD008724 | Pride

miR-200b is associated with cisplatin sensitivity in bladder cancer cells

Project description:We aimed to clarify the role of miR-200b in cisplatin (CDDP) sensitivity in bladder cancer (BCa). CDDP resistant T24 cells (T24RC) were transfected with a miR mimic negative control (NC) or a miR-200b mimic, after which cells were treated with or without CDDP. We found that ectopic miR-200b expression re-sensitized the T24RC cells to CDDP. Gene expression microarray analysis revealed that the combination of miR-200b and CDDP affected genes involved in CDDP sensitivity and cytotoxicity.

2018-05-31 | GSE103250 | GEO

Cdk4-inhibitor induces tumor regression of Bladder cancer in vivo using a metastatic mouse model

Project description:Cdk4/6 inhibitors have shown to increase overall survival in hormone-positive breast tumors, but whether other solid tumors could respond to these inhibitors has not yet defined. Here we show that Palbociclib (a Cdk4/6 specific inhibitor in clinic use) + cisplatin (CDDP, a chemotherapeutic agent most active in locally or advanced bladder cancer patients) treatment exerts antiproliferative effects in vivo using a bladder cancer mouse model.

2018-10-21 | GSE100716 | GEO

Impact of Immune and Stromal Infiltration on Outcomes Following Bladder-Sparing Trimodality Therapy for Muscle-Invasive Bladder Cancer

Project description:Background: Bladder-sparing trimodality therapy (TMT) is an alternative to radical cystectomy (RC) for muscle-invasive bladder cancer (MIBC), and biomarkers to inform therapy selection are needed. Objective: To evaluate immune and stromal signatures in MIBC treated with TMT.

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Impact of molecular subtypes in muscle-invasive bladder cancer on predicting response and survival outcome to neoadjuvant chemotherapy: results from a multi-institutional validation study

Project description:Four different molecular classifications of muscle-invasive bladder cancer (MIBC) based on gene expression have been proposed. With the ultimate goal of utilizing these molecular subtypes for personalized treatment, we investigated their significance in the context of neoadjuvant cisplatin-based chemotherapy (NAC).

2017-05-25 | GSE87304 | GEO

Expression data from bladder tumors and adjacent normal tissues

Project description:miRNAs are involved in cancer development and progression,acting as tumor suppressors or oncogenes. Half of the human miRNAs are located in cancer-associated genomic regions and can function as tumor suppressor genes or oncogenes depending on their targets miRNA profiling was performed on paired bladder cancer tissues and differentially expressed miRNAs were identified in BC and adjacent noncancerous tissues of any disease stage/grade. Ten paired bladder cancer tissues (5 low-grade non-muscle-invasive bladder cancer[NMIBC] and 5 high-grade muscle-invasive bladder cancer[MIBC]) were sent to CapitalBio Corp. (Beijing) for noncoding RNA microarray analysis. The microarray analysis was done as described on the Web site of CapitalBio. NMIBC samples include 07A, 19A, 23A, 24A and T63 while coresponding pairs include 07B, 19B, 23B, 24B and 63. MIBC samples include 10A, 20A, 21A, 34A and 49A while coresponding pairs include 10B, 20B, 21B, 34B and 49B.

2012-07-06 | E-GEOD-39093 | biostudies-arrayexpress

Transcriptional response of ovarian cancer cell lines to HGF and CDDP

Project description:HGF sensitizes ovarian cancer cells to chemotherapeutics, e.g. cisplatin (CDDP), through a signaling cascade activated by its MET oncogene encoded receptor and transduced by the p38MAPK. This cascade results in the regulation of a common set of transcripts in three ovarian cancer cell lines, with different genetic profiles and susceptibility to drugs. In order to elucidate the mechanism of HGF dependent cell sensitization to drugs, the transcriptional response of the three ovarian cancer cell lines to HGF and CDDP were studied by microarray based transcription profiling

2013-12-31 | E-GEOD-24589 | biostudies-arrayexpress

Human bladder cancer cell line high throughput sequencing - genes regulated by hMSH2 - CDDP therapy

Project description:Human bladder cancer cell line high throughput sequencing - genes regulated by hMSH2 - CDDP therapy

| PRJNA797652 | ENA

Bladder-RI

Project description:A Cartes dM-^RIdentite des Tumeurs (CIT) project from the french Ligue Nationale Contre le Cancer (http://cit.ligue-cancer.net/). Seven transcriptome datasets corresponding to a new series of 85 MIBC (Muscle-invasive bladder cancer) and six publicly-available series (298 MIBC) were analyzed. Tumors were classified by consensus clustering. Overall survival was determined from Kaplan-Meier curves. The role of the EGFR pathway was investigated by pathway bioinformatics analysis, determination of the expression levels of its components (by microarray, RT-qPCR and western blot) and of EGFR copy number by CGH arrays. A 40-gene transcriptomic classifier was used to identify basal-like cell lines and a basal-like mouse model. Please note M-^QMIBC molecular subtype': tumors classification using consensus clustering.

2014-06-01 | E-MTAB-1803 | biostudies-arrayexpress

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